Short Communication: Characterization of Madin-Darby Bovine Kidney Cell Line for Peroxisome Proliferator-Activated Receptors: Temporal Response and Sensitivity to Fatty Acids
The peroxisome proliferator-activated receptors (PPAR) are critical for lipid metabolism, and many fatty acids are PPAR agonists. Madin-Darby bovine kidney (MDBK) cells were tested as an in vitro bovine model for PPAR activation, and preliminary evaluation of the effect of fatty acids on bovine PPAR...
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Veröffentlicht in: | Journal of dairy science 2008-07, Vol.91 (7), p.2808-2813 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | The peroxisome proliferator-activated receptors (PPAR) are critical for lipid metabolism, and many fatty acids are PPAR agonists. Madin-Darby bovine kidney (MDBK) cells were tested as an in vitro bovine model for PPAR activation, and preliminary evaluation of the effect of fatty acids on bovine PPAR was performed. Cells were treated with Wy-14643 (WY, specific PPARα agonist) and rosiglitazone (ROSI, specific PPARγ agonist). The gene expression of specific PPARα-responsive genes such as carnitine palmitoyl transferase-1 (CPT1A) and acetyl coenzyme A oxidase (ACOX1) and of PPARγ-responsive gene lipoprotein lipase (LPL) were analyzed using real-time reverse transcription PCR. It was found that CPT1A exhibited a significant increase in cells treated with WY, whereas the ACOX1 gene expression was not altered. The LPL gene expression showed an increase in response to ROSI. Interestingly, LPL was almost undetectable in MDBK cells not treated with ROSI. The potency of different fatty acids in activating PPARα as assessed by CPT1A mRNA abundance in MDBK cells was also tested. The mRNA of CPT1A (2.5- to 1.4-fold) was significantly increased by fatty acids in the order of palmitate>linolenate>linoleate>conjugated linoleate, and oleate. The results demonstrated MDBK cells to be responsive to PPAR agonists and thus a promising model to evaluate the role of PPAR in bovine cells. In addition, fatty acids were proven to have a different potency in modulating expression of CPT1A through PPARα. |
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ISSN: | 0022-0302 1525-3198 |
DOI: | 10.3168/jds.2007-0789 |